To investigate potential mechanisms for the postulated involvement of anti-myocardial cell-surface antibodies in the pathogenesis of human hypertrophic cardiomyopathy (HCM), patients with HCM were assayed by indirect immunoprecipitation for circulating anti-beta-1-receptor autoantibodies. Eight of 18 sera tested resulted in 20-70% precipitation of soulbilized turkey erythrocyte beta-1-receptor under the conditions employed. Further work will establish the prevalence of anti-beta-1 receptor autoantibodies in HCM and salient control populations, characterize the antibody-receptor interaction, and assess the ability of anti-beta-1-receptor autoantibodies to function as beta-adrenergic agnists.